摘要
目的 探讨 SAH后 DCVS及其迟发性神经功能缺损的发生机制。方法 HE和 TUNEL染色检测脑血管内皮细胞、平滑肌细胞及神经细胞增生、凋亡和坏死改变。结果 TUNEL检测发现 SAH后 30 min海马、皮层、及基底节区可见凋亡细胞开始出现 ,血管和神经细胞形态结构基本正常。SAH后 3d凋亡细胞开始增多 ,部分神经细胞核固缩、浓染、染色质集聚 ,血管内皮和平滑肌凋亡细胞开始出现 ,血管外膜可见炎细胞。SAH后 7d凋亡和坏死的神经细胞明显增多 ,而血管在坏死和凋亡的基础上增生性改变更加明显。结论 SAH迟发性脑血管痉挛及其迟发性神经细胞损伤的病理过程中 ,既有细胞坏死 ,也有细胞凋亡的病理生理过程 ,血管内皮细胞和血管平滑肌细胞还有病理性增生的血管重构改变 ,是多种病变形式并存的病理过程。
Objective To elucidate the mechanism DCVS and late response nervous function detection occur Methods Brain vascular vessel, smooth muscle and nerve cells enhancement, necrosis and apoptosis alteration were tested through HE AND TUNEL Results Apoptosis cell began to appear in hippocampus, cortex and basal ganglia 30 minutes after SAH by TUNEL, while the cytoarchitactures of vascular and nerve cells are normal Enhancement of apoptosis cell was found the third day after SAH, part of nerve karyons and chromosome conglomerate, apoptosis in vascular vessel smooth muscle was also found, and inflammatory cells can be seen in vascular exosporium Apoptosis and necrosis cells increased evidently and reached the seventh day after SAH The alteration of enhancement of apoptosis and necrosis of vascular increased Conclusions The pathologic process of late brain vascular hyperkinesias, late response cerebral vasospasm and its late response neural cell lesion include both cell necrosis and cell apoptosis with alteration of hyperplasic of intima of vessel and vascular smooth muscle cell, it is a pathologic course of various lesion and there into apoptosis are fundamental cause of this alteration
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2003年第7期441-442,共2页
Chinese Journal of Gerontology
